. 2014 Apr;88(8):4558–4571. doi: 10.1128/JVI.03431-13

TABLE 1.

Summary of α2β1, GM1, and N-acetylneuraminic acid usage for infection by human rotaviruses

Virus strain	α2β1 usage^a	Untreated cell findings					Infectivity in sialidase-treated cells
		Proposed internalization pathway^c	CTB inhibition of given property^b (% at 1 μg/ml)		Infectivity reduced by Neu5Acα2Me	Infectivity reduced by a-GM1^e (% at 10 mM)	Increased	Reduced by Neu5Acα2Me	Reduced by a-GM1^e (% at 10 mM)
		Proposed internalization pathway^c	VP8* binding^e	Infectivity	Infectivity reduced by Neu5Acα2Me	Infectivity reduced by a-GM1^e (% at 10 mM)	Increased	Reduced by Neu5Acα2Me	Reduced by a-GM1^e (% at 10 mM)
RV-5	+	CE	ND	29	−^e	ND	+^e	+^e	ND
Wa	+	CE	21	48	−^d	57	+^d	+^d	35
RV-3	−	ND	39	41	−^e	49	+^e	+^e	43
S12/85	−	ND	ND	48	−^e	ND	+^e	−^e	ND

Shown in references 8, 15, 18, 32, and 35. The extent of α2β1 usage is not affected by sialidase treatment of cells, as shown in this study.

Shown in this study and reference 31 for Wa. GM1 usage also was shown by STD NMR detection of a-GM1 binding by Wa VP8* (31) and RV-3 VP8* (this study). CE, clathrin-mediated endocytosis; ND, not determined.

Data are from references 11 to 13. DS-1 uses CE (12). RV-5 and DS-1 share the G2P1B serotype, differing in VP8* sequence at amino acid positions 82, 89, and 160, so RV-5 also may enter cells by CE.

Shown in this study and reference 31.

Shown in this study.